Initial genetic evidence in mice suggested that Beclin-1 functions as a haplo-insufficient tumor suppressor and that its mono-allelic deletion leads to spontaneous tumors and upon re-expression, it restores autophagy and suppresses tumorigenesis.21, 22 Although Beclin-1 and LC3 are important mediators of autophagy, other molecules and signaling pathways (for example, p53, PI3K/AKT/mTOR) require critical examination to determine their roles in cells' autophagic capacity toward cell death or survival following various triggers. The gene discussed is BECN1; the disease is neoplasm.